The basis for the recommendations to reduce fat and saturated fat is the Diet-Heart Theory which is generally accepted by the medical and public health bodies.  Essentially it concludes that the concentration of total cholesterol in the blood (TC) is a risk factor for heart disease. It follows from this that any factor which increases TC will increase the chances of dying from heart disease. By the same logic anything that reduces TC will also reduce the risks of heart disease.

Saturated fat (SFA) is considered to increase TC and therefore increase the risk of developing heart disease whereas polyunsaturated fat (PUFA) is believed to have the opposite effect and will therefore reduce the risks. These are the precise grounds for concluding that SFA is ‘’bad’’ and should therefore be reduced and PUFA is ‘’good’’ and an increase would be beneficial to health.

The NHS in the UK has endorsed this rationale.

According to the NHS Choices website, TC should be lowered because there is evidence which:

strongly indicates that high cholesterol can increase the risk of:

narrowing of the arteries (atherosclerosis), heart attack , stroke , mini-stroke

This is because cholesterol can build up in the artery wall, restricting the flow of blood to your heart, brain and the rest of your body. It also increases the chance of a blood clot developing somewhere.”

It goes on to say that:

Your risk of coronary heart disease (when your heart’s blood supply is blocked or disrupted) also rises as your blood’s cholesterol level increases and this can cause angina during physical activity.”

People with a raised TC are advised to take steps to lower it in order to reduce the risks of death due to heart disease. To achieve this, the advice is:

to maintain a healthy, balanced diet. It is important to keep your diet low in fatty food, especially food containing saturated fat, and eat lots of fruit, vegetables and wholegrain cereals. This will also help to prevent high cholesterol from returning.”

More specifically:

Eating a healthy diet that is low in saturated fats can reduce your level of LDL (bad cholesterol).

Try to avoid or cut down on the following foods, which are rich in saturated fat: fatty cuts of meat and meat products, such as sausages and pies butter, ghee and lard, cream, soured cream, creme fraiche and ice cream, cheese, particularly hard cheese, cakes and biscuits, chocolate ,coconut oil, coconut cream and palm oil”

Clearly this advice is quite categorical with specific instructions on how to comply with it.

However as I will demonstrate below it is fundamentally flawed.

The focus of the official advice is restricted to heart disease. Anyone who takes steps to implement this advice needs to be totally confident that there will be not be increase in other causes of death. The critical factor should be all-cause mortality not one particular disease. Therefore it is highly relevant that when the relationship between all-cause mortality and TC is examined a totally different picture emerges. The results of a study conducted in the West of Scotland are particularly relevant. From 1972 to 1976, 7,053 men and 8,346 women aged 45 to 64 were recruited in Renfrew and Paisley. A range of parameters including TC was measured and arrangements made for deaths to be recorded and information on the cause of death supplied to the research team. The results are shown in Figure 1.



Note: The cholesterol in the blood may be analysed in the serum or in the plasma as indicated above.

These results confirm that in both men and women the death rate from coronary heart disease (CHD) does increase with TC level. However for cancer the reverse is true so that the death rate increases as the TC falls. As a consequence there is no simple relationship between all-cause mortality and TC levels. For men the death rate is relatively high when the TC is below 5mmol/L but does not change at the higher TC levels. For women the graph is ‘’U’’ shaped with the minimum at about 7mmol/L. The possibility that the low TC level could be caused by the cancer which may have been present or unsuspected at the time of the recruitment was considered. However it was found that if any cancer cases which were diagnosed in the first 4 years of the study were excluded, the inverse relationship between TC and cancer persisted.  Therefore it can safely be concluded that the TC is not an effect of the developing cancer.

The researchers concluded that although a reduction of TC in men may help to control CHD it is frequently found that the all-cause mortality is unchanged. Furthermore it may well be a mistake to assume that advice to the general population to reduce the consumption of saturated fat will necessarily lead to any reduction in all-cause mortality(1).

In 1992 a major conference in the U.S.A was presented with results from a range of different countries which confirmed that there was an increased death rate from all causes at low TC levels (Table 1). In particular there was a significantly increased risk of non-cardiovascular deaths in both men and women with TC levels below 160 mg/100ml(4mmol/L) for a variety of different causes. Men had a 20% higher rate of cancer deaths than those in the TC range of 160 to 199 mg/100ml. There were also increased death rates for non-cancer non-CVD (35%), respiratory system conditions (15%), digestive system conditions (50%) and ‘’other causes’’ (70%). For both respiratory and digestive system death rates there was a graded response with TC levels ie the death rate declined as the TC increased. This relationship continued above 200 mg/100ml(5mmol/L). Among women, the picture was similar except that the excess cancer mortality was smaller at about 5%. In men it was clear that there was a direct relationship between death rate due to CHD and TC level ie the higher the TC level the greater the death rate.

However in women a raised TC level is not associated with any increase in all-cause mortality or even an increase in CHD mortality. Clearly the relatively high death rates at the low levels of TC were a direct challenge to the accepted views which prevailed at the time. The earlier findings primarily based on middle-aged men that a raised TC was associated with increased risks of death from CHD had been the justification  for prescribing drugs to lower in the TC in the blood. Hence various suggestions were proposed which would essentially discredit or explain away the new information that was ‘’inconvenient’’ for those who were keen to maintain the status quo. Once again it was suggested that the low cholesterol was actually an early sign of the emerging disease. In other words the low cholesterol was an effect of the disease not the cause. This possibility was ruled out by the fact that if the results for any individual who died during the first 5 years of the study were excluded from the analysis, the results were not changed (2).


TC, Mmol/L (mg/100ml) Men Women
>4.1 (160) 1.17 1.10
4.1-5.2 (160-200) 1.00 1.00
5.2-6.2 (200-240) 1.02 0.94
>6.2 (240) 1.14 0.97

In the same year results from a major US project (MRFIT) in which over 350,000 middle-aged men were monitored confirmed that the all-cause mortality increased at low TCs. (Figure 2). In particular, TC levels below 4.14mmol/L were associated with increased risk of death from cancer of the liver and pancreas, digestive diseases, suicide and alcohol dependency syndrome(3).





3.The limitations of concentrating on information from middle-aged men have been highlighted by results from the Framingham Study which relate to older men.  Based on data from 5209 men and women recruited in the period up to 1980 it was observed that the relationship between TC and all-cause mortality was positive at age 40, negative at age 80 and negligible at ages from 50 to 70 years. The authors of the report concluded that:

’Physicians should be cautious about initiating cholesterol-lowering treatment in men and women above 65 to 70 years old.’’


1. C. G. Isles et al (1989) British Medical Journal  298 pp.920-924.

2. D. Jacobs et al (1992).Report on the Conference on Low Blood Cholesterol: Mortality Associations Circulation 86, pp1046-1060.

3. J.D. Neaton et al (1992) Archives of Internal Medicine 152(7) pp.1490-1500

4. R A Kronmal et al (1993) Arch Int Med 153 (9)  pp1065-73.



 Part 2 to follow soon!